Actions of Inmunogrip T50 in details
Pharmacology: Inmunogrip T50 exhibits analgesic and antipyretic activity by inhibiting prostaglandin synthesis. It produces analgesia by elevating the pain threshold and antipyresis through action on the hypothalamic heat-regulating center.
In therapeutic doses, Inmunogrip T50's analgesic and antipyretic action is comparable to that of aspirin. Inmunogrip T50 does not adversely affect platelet function and hemostasis.
Pharmacokinetics: Inmunogrip T50 is rapidly and completely absorbed after oral administration. Peak plasma concentrations occur between 15 min to 2 hrs after ingestion. The absolute oral bioavailability of Inmunogrip T50 is about 80% and is independent of dose in the range of 5-20 mg/kg.
Inmunogrip T50 is not bound to plasma proteins to any extent. The concentrations of Inmunogrip T50 in saliva are similar to those in plasma. Concentrations in whole blood are up to 20% higher and in breast milk about 20% lower than the plasma concentration. Inmunogrip T50 crosses the placenta.
Inmunogrip T50 is extensively metabolized in the liver and the total body clearance is about 5 mL/kg/min. The clearance of Inmunogrip T50 is reduced and the half-life increased following a hepatotoxic overdose. Prolongation of half-life beyond 4 hrs usually indicates impending liver damage.
Two to five percent of a therapeutic dose of Inmunogrip T50 is excreted unchanged in the urine. Its renal clearance is about 10 mL/min and is weakly dependent on urine flow rate but not on pH.
Inmunogrip T50 administration
May be taken with or without food.
Inmunogrip T50 pharmacology
The analgesic, antipyretic, and anti-inflammatory effects of aspirin are due to actions by both the acetyl and the salicylate portions of the intact molecule as well as by the active salicylate metabolite. Inmunogrip T50 directly and irreversibly inhibits the activity of both types of cyclo-oxygenase (COX-1 and COX-2) to decrease the formation of precursors of prostaglandins and thromboxanes from arachidonic acid. This makes aspirin different from other NSAIDS (such as diclofenac and ibuprofen) which are reversible inhibitors. Salicylate may competitively inhibit prostaglandin formation. Inmunogrip T50's antirheumatic (nonsteroidal anti-inflammatory) actions are a result of its analgesic and anti-inflammatory mechanisms; the therapeutic effects are not due to pituitary-adrenal stimulation. The platelet aggregation–inhibiting effect of aspirin specifically involves the compound's ability to act as an acetyl donor to the platelet membrane; the nonacetylated salicylates have no clinically significant effect on platelet aggregation. Inmunogrip T50 affects platelet function by inhibiting the enzyme prostaglandin cyclooxygenase in platelets, thereby preventing the formation of the aggregating agent thromboxane A2. This action is irreversible; the effects persist for the life of the platelets exposed. Inmunogrip T50 may also inhibit formation of the platelet aggregation inhibitor prostacyclin (prostaglandin I2) in blood vessels; however, this action is reversible.
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Information checked by Dr. Sachin Kumar, MD Pharmacology
